ASMR

What Causes ASMR?

The exact cause of ASMR responses is not known at present. Scientific studies have produced some evidence that AMSR triggers induce a measurable physical or neurological reaction in some people, but the neurological mechanism of the reaction hasn’t been identified.

Some theories of the science behind ASMR include:

• Personality traits. Some studies have associated ASMR responses with specific personality traits described by the Big Five Personality Inventory, a model commonly used by psychologists and psychiatrists to describe personality. The studies have found that people who experience ASMR are more likely to exhibit high scores in Neuroticism and Openness and low scores in Conscientiousness, Extraversion, and Agreeableness. Broadly, this means that people who experience ASMR are more likely to be creative and experience anxiety and mood swings. They are less likely to enjoy socializing or to take interest in others.
• Placebo effect. Some scientists think that ASMR may be an example of a placebo effect, meaning that some people feel pleasurable responses to ASMR triggers because they expect to feel them. However, this does not mean that the reactions are not real.

Is ASMR Hereditary?

There is currently no evidence of a genetic connection to ASMR. However, some researchers think ASMR is similar to synesthesia, a condition that may have a genetic component. Some studies have suggested that people with a family history of synesthesia have a higher probability of having the condition themselves, suggesting a possible inherited component. However, scientists have not yet identified a single gene definitively associated with synesthesia. Sometimes a genetic predisposition may work in combination with environmental factors to trigger the condition.

How Is ASMR Detected?

Little is known about the origin of ASMR. It’s not clear whether people are born with the ability to experience its effects or whether the ability can develop later.

How Is ASMR Diagnosed?

Because ASMR is not considered to be a neurological disorder, there is no standard way to diagnose it. If a patient seeks a diagnosis for their ASMR symptoms, a doctor will likely start with a physical exam to rule out other problems that may be causing the symptoms. After these exams, if the doctor suspects that a medical or mental health-related issue is the cause of the symptoms, they may recommend other assessments to solidify the diagnosis.

Diagnostic steps may include:

• A physical exam. This exam aims to rule out physical conditions that could be causing the symptoms.
• Neurological tests. These tests measure the function of the patient’s nervous system. They evaluate functions such as balance, reflexes, memory, visual perception, and language.
• Assessment tools. Assessment tools designed to identify similar conditions, such as synesthesia, measure a person’s response to visual and auditory stimuli. The tests are usually administered more than once to determine if the person’s perceptions are consistent. Predictable sensory experiences are a key characteristic of actual synesthesia.

PLEASE CONSULT A PHYSICIAN FOR MORE INFORMATION.

How Is ASMR Treated?

ASMR usually requires no treatment, and there are no known treatment approaches that can change a person’s sensory experiences. Although some people with ASMR may experience some distress or impairments associated with their sensory experiences, most people with the condition describe it as a positive experience. 

How Does ASMR Progress?

It is unclear whether ASMR effects change over time or whether they can become more or less intense with increased attention or exposure to triggers. Some people have reported decreased sensitivity to ASMR triggers with overexposure to the stimuli, but these are anecdotal reports, not scientific studies.

How Is ASMR Prevented?

There is no known way to prevent ASMR. For those who prefer not to experience the phenomenon, avoidance of known triggers is the best strategy.

ASMR Caregiver Tips

The association of ASMR with certain personality traits suggests that ASMR may exist alongside other mental health and brain-related conditions, a situation called co-morbidity. Some studies have found that ASMR may be associated with susceptibility to anxiety, raising the possibility of an increased risk of anxiety disorders.

ASMR Brain Science

So far, only a few studies have attempted to find a neurological basis for ASMR responses. Results of these studies have suggested some brain differences in people who experience ASMR, although some of the results have been inconsistent from study to study.

Some possible brain differences include:

• People sometimes show increased activity in their medial prefrontal cortex during ASMR responses. This part of the brain is involved in sensory processing, attention, and social behavior.
• One study found increased activity in the nucleus accumbens, part of the brain’s reward system. The nucleus accumbens plays a role in pleasurable sensations and determining whether we “like” a stimulus.
• Multiple studies have suggested a negative association between ASMR experiences and activity in brain areas associated with attention and executive function. This suggests people may be impaired in their ability to do tasks requiring focused attention during or after their ASMR experiences.

ASMR Research

Title: Investigating the Mechanisms of the Effects of Psilocybin on Visual Perception and Visual Representations in the Brain

Stage: Not Yet Recruiting

University of California, Berkeley

Berkeley, CA  

The long-term objective of this project is to characterize how psilocybin affects visual perception and the brain’s representation of the visual environment. Researchers know psilocybin alters aspects of visual perception, but the underlying brain mechanisms contributing to these effects are poorly understood. The proposed work will address these questions in a large, diverse sample of healthy human subjects by using functional magnetic resonance imaging (fMRI) to measure the brain’s responses to visual stimuli. The proposed research will document which brain areas mediate the effects of psilocybin. The technique of fMRI will be employed to measure brain activity in different brain areas while subjects are performing a visual perceptual task.

Title: Intrathecal Morphine Microdose Method Sensory Changes

Stage: Recruiting

Contact: Denise Wilkes, MD-PhD

University of Texas Medical Branch

Galveston, TX 

The use of intrathecal drug delivery systems for managing chronic non-cancer pain has been in practice for over 30 years. A recently published study from the University of Texas Medical Branch performed a retrospective review of the morphine microdose method in community-based clinics. The goal of the study was to examine the morphine microdose method in an outpatient setting and assess the success of therapy, pain scores, and dose escalation. Patients were successfully weaned off their systemic opioids, maintained in an opioid-free period for 4-6 weeks, and then underwent a microdose trial and implantation. The majority of patients were successfully managed on morphine monotherapy, with a significant reduction in pain scores, and dose escalations comparable to prior studies. No prospective studies have examined the microdose method in correlation with changes in pain sensitivity.

Several studies have looked at the use of various pain testing models to investigate the effects of chronic opioid therapy and changes in pain perception. A systematic review of the literature identified clinical studies incorporating measures of hyperalgesia in patients on chronic opioid therapy. This review aimed to find the optimal testing modality to evaluate pain threshold and tolerance to external stimuli, including mechanical (pressure, touch, injection), thermal (cold/heat), and electrical. Although the results did not reveal any one method with sufficient power, several prospective studies evaluating hyperalgesia with heat pain ratings have shown some promising results; two studies revealing significant changes in heat responses for opioid treatment groups, and one study demonstrating lower heat pain perception values following an opioid taper. The latter study of research pertaining to pain sensitivity changes following an opioid taper is lacking, and only recently was a study performed investigating changes in pressure threshold following the transition from full mu agonist to buprenorphine. At this juncture, little is known about how pain thresholds change due to opioid dose changes and/or route of delivery changes, such as oral to intrathecal routes.

Title: Neural Correlates of Sensory Phenomena in Tourette Syndrome

Stage: Recruiting

Principal Investigator: David A. Isaacs, MD

Vanderbilt University Medical Center

Nashville, TN

Tourette syndrome (TS) is a multifaceted disorder that affects 0.6-1% of the global population. Across the lifespan, individuals with TS suffer worse quality of life (QOL) than the general population. While tics are the defining feature of TS, it is the widespread psychiatric and sensory symptoms that exert a greater impact on QOL: more than 85% of individuals with TS are diagnosed with a psychiatric disorder, and 90% experience distressing sensory symptoms. The latest TS disease models and practice guidelines account for common psychiatric symptoms, but sensory symptoms remain under-recognized and under-studied. Progress in understanding and treating TS requires deepening insight into the disorder’s sensory dimension.

The most pervasive sensory manifestation of TS is sensory over-responsivity (SOR). SOR is defined as an excessive behavioral response to commonplace environmental stimuli. SOR is associated with avoidant behavior and functional impairment. More than 50% of children and 80% of adults with TS report SOR. Across age groups, SOR is positively correlated with the severity of tics and psychiatric symptoms and negatively correlated with QOL. Thus, SOR is an integral facet of the TS phenotype, one intertwined with core elements of the disorder and worse QOL. This proposal seeks to clarify the mechanistic bases of SOR in TS (Aims 1 and 2).

An enhanced understanding of SOR’s neurobiological basis is crucial to a more complete knowledge of TS pathophysiology. Two neurophysiologic mechanisms are implicated in SOR: sensory gating impairment and autonomic hyperarousal. Sensory gating is the physiologic process whereby redundant environmental stimuli are filtered out in the early stages of perception. Impairment of sensory gating gives rise to altered sensory perception. Autonomic hyperarousal is a state of excessive sympathetic tone and/or reduced parasympathetic tone, which hampers behavioral adaptation to sensory input. In TS, multiple lines of evidence suggest both sensory gating and autonomic function are impaired. However, prior investigations have suffered from methodologic limitations and have not examined the link between neurophysiologic dysfunction and sensory symptoms.

Aim 1. Identify an electroencephalographic (EEG) signature of SOR in TS. Hypotheses: (1a) Relative to healthy controls, TS adults exhibit impaired sensory gating; (1b) the extent of impaired sensory gating in TS correlates with the degree of SOR. We will recruit 60 TS adults and 60 age- and sex-matched healthy controls to complete rating scales for SOR, psychiatric symptoms, and tics. Subjects will then be monitored on dense-array scalp EEG during sequential auditory and tactile sensory gating paradigms.

Aim 2. Identify an autonomic signature of SOR in TS. Hypotheses: (2a) Relative to healthy controls, TS adults exhibit autonomic hyperarousal in response to non-aversive sensory stimuli; (2b) extent of autonomic hyperarousal correlates with SOR severity in TS. Heart rate and electrodermal activity will be monitored during the Aim 1 sensory gating paradigms and a 10-minute rest period. Heart rate variability and electrodermal activity will serve as indices of parasympathetic and sympathetic activity, respectively.

Impact: Results will clarify the extent of sensory gating impairment in TS, the nature of autonomic dysfunction in TS, and the clinical correlates of neurophysiologic dysfunction in TS.